Uncommon Descent Serving The Intelligent Design Community
LPA

Life Project Architecture

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

A point that Darwinists make is that anti-Darwinists have not developed any theory for the origins of species, and think that is a weakness. But for an IDer/creationist is not so difficult to have ideas about solutions of the problem of origins. I for one developed a proposal for a theory, and I will illustrate it here. I called it “LPA” (Life Project Architecture). See below its simple schema, where the x-axis is time and the y-axis the top-down intelligent causation:

LPA model for origins is cent percent design based. The role of natural selection, about the creation of biological information and complexity, is null. To grasp LPA one must entirely invert the reasoning of evolutionism. This means in the same time to assume a solid informatics engineering perspective and apply it to biology.

 

An axiom of Darwinism is the corporeal descent of all species from a simple unique corporeal common ancestor, by means of unintelligent processes. To pass to LPA this axiom has to be somehow inverted and becomes: abstract descent of all kinds from a unique complex abstract common archetype-kind, in the context of a global integrated project of life on Earth. While in Darwinism all the core stuff happens only at the corporeal level, in LPA it happens at the incorporeal level. The inversion of LPA compared to Darwinism not only substitutes non intelligent causes with intelligence but considers two layers upon the corporeal layer, the only one considered by materialist evolutionism. Darwinism is one-dimensional, LPA is three-dimensional.

 

This inversion of LPA vs. Darwinism (which in a sense is a restoration of truth) immediately removes the major absurdities and problems of evolutionism:

(1) Intelligence, able to create information and organization, substitutes chance and necessity, which are unable.

(2) The “less” comes from the “more” and not the opposite, as in evolutionism.

(3) The corporeal macroevolution, which is a real “engineering suicide”, is substituted with an abstract incorporeal derivation, done at a higher layer than the material one. The bodies have no more to materially and monstrously morph, with all the countless complications one can imagine.

(4) The Darwinian material common ancestor of minimal complexity becomes the immaterial template of the more complex being, from which all the simpler beings abstractly derive as sub-projects, when some major characteristics and architectural plans are changed.

(5) What is intelligent is created by intelligence. It is obvious that the unintelligent cannot produce the intelligent, as evolutionism pretends.

(6) The incapability of chance and necessity to create semiotic processing, sophisticated molecular machinery, CSI, correlated CSI, irreducible complexity, functional hierarchies, etc.

Who is the more complex living being that can pretend to be the “maximum project template” in LPA? Answer: man. Before this answer Darwinists object that man arose last in history, then cannot be first. In LPA man can well be the first in the order of design and last in the order of time. Conversely, bacteria, which are the simplest organisms, are last in the order of design and first in the time order. In fact, you can see in the middle of the schema, at the incorporeal layer, the possibility of a total scrambling between design order and time order. This is the flexibility that informatics shows so well. By the way, it is indeed the appearance over time from the simplest to the more complex species that caused the illusion of an evolution from simplicity to complexity, while instead it was simply a specific order of execution of a complexity already fully present from the beginning in the design incorporeal layer.

The LPA explains also all homologies, analogies and similarities between all living beings, at the genetic, morphological, functional and system levels, because LPA implements very strong “common design” “shared libraries” “high level integration” “software reuse” paradigms. In fact, in the schema, at the top level, you see the shared libraries (genotypic and phenotypic) strongly interrelated each other and in turn with the core design, by means of a tri-way bus/channel.

LPA entails three layers: archetypical, incorporeal and corporeal (on the left side of the schema). They are related in the informatics jargon (on the right side) to: design, installation and deployment, execution. The design phase deals with the “sources”, the installation phase deals with “executables” and the execution phase involves “processes” and outputs. Any computer programmer will recognize the standard iter of informatics engineering. LPA could quite well represent how an informatics or robotics engineer, in charge of developing a series of different robots, would organize the overall project, according to a high-level integrated vision. Warning: here I don’t affirm that living beings are simple robots. They are far higher and more complex than robots. But this, to greater reason, reinforces the ID argument, because this implies that their design and construction must be far more sophisticated than modern robotics.

The shift of the job from matter to abstractness, which greatly increases the flexibility, is a fundamental engineering principle, which LPA implements. The history of engineering and technology shows us that engineers have always strived to shift their job from matter to mind. Today engineers use high level abstract tools (CAE, CAD, CAM, etc.). No engineer would use directly low level Darwinian material evolution. Darwinism is a decrepit bankrupt way of thinking, unable to construct the least system. ID LPA is a modern and technologically sound way to construct complex systems.

Another point about LPA is that it agrees with engineering and in the same time is consistent with traditional cosmogony (when is correctly interpreted), according to which the manifestation of macrocosms and microcosms (which are analogous and share the same layering) is a top-down causation ID process that starts from archetypical principles, passes trough an intermediate incorporeal formation and finally concludes into the corporeal world. In LPA the teaching of tradition about creation and engineering meet. Not by chance or by my invention, rather because both describe complex constructions of intelligence. All sciences of construction necessarily share some basic principles that are universal. LPA meets such principles.

Also about the position of man in nature LPA is inverted respecting evolutionism because is “man-centric”. Here again tradition and engineering meet. In any traditional doctrine man is the “imago-Dei” “center of creation”, the hierarchically higher being who synthesizes in himself all others lower peripheral beings. Analogously, if an engineer wants to construct – say – a computer, he starts to think about the central processing unit, then he will develop the peripheral devices.

An important point is why I called the living beings as “kinds”, K0, K1, K2… in the LPA model. The high level design at the archetype layer doesn’t need to specify in advance and in details all the countless species, variants and races of a kind. These variants will differ from the parent kind only in some minor details, while kinds differ in major architectural body plan aspects. What is sufficient is to carefully design and insert into a set of main kinds the complex potentialities needed to generate their minor variants during reproduction of populations in history, by means of endogen and hexogen triggering signals or factors at run time. In few words, the biological “software” must be highly flexible and parametrized, scalable, allowing plasticity and micro-evolvability. I called “microevolution trees” the trees of variants for each kind K and I symbolized them with triangles inside the final corporeal layer. I believe it is sensible to identify the Ks to what in the classic taxonomy are families/kinds. Also most creationists agree on that. As example, Nathaniel T. Jeanson writes “reproductive compatibility identifies membership within a kind. Breeding experiments identify the classification rank of family (kingdom-phylum-class-order-family-genus-species) as roughly defining the boundaries of each kind”. This level is roughly the threshold below which microevolution trees begin.

What evidences support LPA? To my knowledge, the main biological data known so far – if you dismiss the evolutionist eyeglasses – fit well with LPA, because common design explains all things that Darwinian common descent seems to explain. With the difference that LPA has not the absurdities and contradictions that Darwinism has.

Comments
Johnathan M. Have you ever rebutted this take on your ERV articles? It was shown to me 2 days ago. Thank you in advance. http://www.evolutionarymodel.com/evolutionnews.htm David Buzulak (Evolution Myth on Facebook)Buzulak
February 5, 2014
February
02
Feb
5
05
2014
12:45 PM
12
12
45
PM
PDT
I can certainly understand the idea of there being a grand 'construction' project in mind for which smaller, support systems must first be implemented. And certainly, in the case of human beings, some of those preliminary steps would have to be taken and allowed to progress to a sufficient level. I'm thinking of things like oxygen levels, food sources, etc. I'll try and have a better think about this and see if I can justify the immense time involved. But it does seem to me that, inherent in your model, is a not all-powerful designer, i.e. one that could not just 'create' the whole living biosphere in one go. I'm just trying to get my head around what kind of tools the designer used and/or had available and/or was capable of using. Getting a handle on the design implementation techniques would help explain some of the data we see in the fossils, the genomes, the observed morphology and the bio-geographic distribution of species. But interesting!Jerad
September 24, 2013
September
09
Sep
24
24
2013
01:45 AM
1
01
45
AM
PDT
Shogun #31
Here is an interesting thought, given the centrality of humans in this picture, this could also mean that the incorporeal design phase can be stretched back all the way to the initial fine-tuning of the big bang. Which means that the designing process deals with not only Earth-bound biological variables, but also with a much larger array of universal variables.
That's true, and worth of future investigations. Sure the shared libraries must contain also what you call "a much larger array of universal variables".niwrad
March 15, 2013
March
03
Mar
15
15
2013
04:38 AM
4
04
38
AM
PDT
thanks BA77, that is a good interview.lifepsy
March 14, 2013
March
03
Mar
14
14
2013
10:49 AM
10
10
49
AM
PDT
Just the interview portion with Dr. Lightner is here: The definitive response on ERV's and Creation, with Dr. Jean Lightner http://www.youtube.com/watch?v=feHYEgzaGkYbornagain77
March 14, 2013
March
03
Mar
14
14
2013
03:43 AM
3
03
43
AM
PDT
lifepsy you may be interested in this video clip, where Ian Juby interviews Dr. Jean Lightner and they clearly lay out, for the layman, what the ERV argument is and exactly why the ERV argument from Darwinists is now falsified: ERV's - Dumb DNA design? - Ian Juby - February 2013 - video http://www.youtube.com/watch?feature=player_detailpage&v=bLx8NnhRdC4#t=768sbornagain77
March 14, 2013
March
03
Mar
14
14
2013
03:38 AM
3
03
38
AM
PDT
lifepsy, thanks for the links. ,,, It is one thing to just proclaim something to be true as Darwinists continually do, it is quite another to empirically back it up.bornagain77
March 14, 2013
March
03
Mar
14
14
2013
03:17 AM
3
03
17
AM
PDT
Mung???
How do empirical observations “predict” anyth8ing at all? It seems to me that you don’t know what you’re talking about.
and yet I had cited @ 42:
“The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable.” - Michael Behe – The Edge of Evolution – page 146
Did Dr. Behe make a 'prediction' about what we should expect to find from the empirical evidence or not? ,,, And why this irrational antagonism towards me from you on this and the other thread? This irrationality is uncharacteristic of you.bornagain77
March 14, 2013
March
03
Mar
14
14
2013
03:11 AM
3
03
11
AM
PDT
Genomicus #48
"Sure, but it [functional but unnecessary proteins] is not predicted by the LPA model, while it is predicted from front-loading. Thus, front-loading appears to me to be a superior ID hypothesis. In other words, the LPA model – like Darwinian evolution – must explain this pattern through ad hoc adjustments."
In my short description of the LPA model (1345 words, it's a blog after all) I didn't include that "prediction" because it was implicit. LPA is a cent percent informatics based model and it was absolutely trivial to waste words to say that in informatics there are "functional but unnecessary subroutines", exactly as to say there are bits. I think that LPA has the pros of your macroevolutionary front-loading but has not the cons. Likely here is the point, our disagreement is that, despite of we are two IDers, you believe in corporeal macroevolution while I don't.niwrad
March 14, 2013
March
03
Mar
14
14
2013
01:33 AM
1
01
33
AM
PDT
Genomicus
In other words, the ERV sequences aren’t located in the same genomic loci across different taxa. This is what matters
If you're suggesting ERVs found in similar loci is indicative of common descent, there are many studies suggesting non-random and preferential positioning of retrovirus sequences. This kind of data refutes the claims of re-used ERV sites having to be an 'amazing coincidence' if not by common descent. Perpetually mobile footprints of ancient infections in human genome http://www.sciencedirect.com/science/article/pii/S0014579398004785 Although not available for HERVs at this point, the results for other retroelements demonstrate that transcriptionally active genome regions might be preferred targets for retrovirus integration and that the site selection during retroposition can be influenced by many factors A good example of retroelement–host interaction gives the study of de novo insertions of Ty1 and Ty3 yeast retrotransposons that are analogues of endogenous retroviruses. Most of the integration sites were found clustered upstream of the genes transcribed by RNA polymerase III. There were identified `hot spots' containing integration sites used up to 280 times more frequently than predicted mathematically. A recent study of the de novo retroviral integration demonstrated also preference for scaffold- or matrix-attachment regions (S/MARs) flanked by DNA with high bending potential. Integration specificity of the hobo element of Drosophila melanogaster is dependent on sequences flanking the integration site http://link.springer.com/article/10.1023%2FA%3A1003712619487 We analyzed the integration specificity of the hobo transposable element of Drosophila melanogaster. Our results indicate that hobo is similar to other transposable elements in that it can integrate into a large number of sites, but that some sites are preferred over others, with a few sites acting as integration hot spots. Large-scale discovery of insertion hotspots and preferential integration sites of human transposed elements http://nar.oxfordjournals.org/content/38/5/1515.full We first discovered that most TEs insert within specific ‘hotspots’ along the targeted TE... Finally, we performed a global assessment to determine the extent to which young TEs tend to nest within older transposed elements and identified a 4-fold higher tendency of TEs to insert into existing TEs than to insert within non-TE intergenic regions. Our analysis demonstrates that TEs are highly biased to insert within certain TEs, in specific orientations and within specific targeted TE positions. TE nesting events also reveal new characteristics of the molecular mechanisms underlying transposition. Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0020234 Chromosomal regions rich in expressed genes were favored for HIV integration, but these regions were found to be interleaved with unfavorable regions at CpG islands. MLV vectors showed a strong bias in favor of integration near transcription start sites, as reported previously. ASLV vectors showed only a weak preference for active genes and no preference for transcription start regions. Thus, each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection. Integration of retroviral vectors http://www.sciencedirect.com/science/article/pii/S095279151200129X Several members of the retrovirus family show distinct pattern for preferential integration into the host genome. Despite many years of investigation, precise mechanisms of target site selection and the fundamental interplay of viral integrase and host cell proteins are still unknown.lifepsy
March 13, 2013
March
03
Mar
13
13
2013
09:07 PM
9
09
07
PM
PDT
BA77:
So Genomicus, it doesn’t bother you in the least when the math, experimental, and empirical, evidence ‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life???
You forgot to include all the links that would allegedly make the argument that you only claim to make.
1) Math...‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life
So?
2) experimental evidence ‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life
How so?
3) empirical, evidence ‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life?
How do empirical observations "predict" anyth8ing at all? It seems to me that you don't know what you're talking about.Mung
March 13, 2013
March
03
Mar
13
13
2013
08:32 PM
8
08
32
PM
PDT
More on ERV's The Nucleotide Sequence of Koala (Phascolarctos cinereus) Retrovirus: a Novel Type C Endogenous Virus Related to Gibbon Ape Leukemia Virus http://jvi.asm.org/content/74/9/4264.short KoRV (Koala retrovirus) paradoxically clusters with gibbon ape leukemia virus (GALV). The strong similarity between GALV and KoRV suggests that these viruses are closely related and that recent cross-host transmission has occurred. ^^^Koala and Gibbon HGT Interclass Transmission and Phyletic Host Tracking in Murine Leukemia Virus-Related Retroviruses http://jvi.asm.org/content/73/3/2442.short ..two recent instances of transmission of zoonotic infections between distantly related host organisms were identified. One, from mammals to birds, has led to a rapid adaptive radiation into other avian hosts. The other, between placental and marsupial mammals, involves viruses clustering with recently described porcine retroviruses Multiple Groups of Endogenous Betaretroviruses in Mice, Rats, and Other Mammals http://jvi.asm.org/content/78/11/5784.short We propose a model whereby betaretroviruses have been evolving within the genomes of murid rodents for at least the last 20 million years and, subsequent to (or concomitant with) the global spread of their murid hosts, have occasionally been transmitted to other species. ^^^Mice Bat HGT Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes: Probable Transmissions between Other Primates and Chimpanzees http://jvi.asm.org/content/80/3/1367.short We screened both the human genome (version hg16) and the chimpanzee genome (version PanTro1) for ERVs and conducted a phylogenetic analysis of recent integrations. We found a number of recent integrations within both genomes. They segregated into four groups. Two larger gammaretrovirus-like groups (PtG1 and PtG2) occurred in chimpanzees but not in humans. The PtG sequences were most similar to two baboon ERVs and a macaque sequence but neither to other chimpanzee ERVs nor to any human gammaretrovirus-like ERVs. The pattern was consistent with cross-species transfer via predation. This appears to be an example of horizontal transfer of retroviruses with occasional fixation in the germ line. Porcine endogenous retrovirus integration sites in the human genome: features in common with those of murine leukemia virus. http://www.ncbi.nlm.nih.gov/pubmed/16928752 All these results show similarities between PERV and murine leukemia virus integration site selection, suggesting that gammaretroviruses have a common pattern of integration and that the mechanisms of target site selection within a retrovirus genus might be similar. ^^^ ERV sites not random The distribution of endogenous chicken retrovirus sequences in the DNA of galliform birds does not coincide with avian phylogenetic relationships. http://www.ncbi.nlm.nih.gov/pubmed/225036 Domestic chickens carry the genome of the endogenous retrovirus RAV-O as DNA sequences integrated into host chromosomes transmitted through the germ line.... No fragments with sequences related to chicken retroviruses were found, however, in digests of DNA prepared from Sonnerat's, Ceylonese and Green Junglefowl, from two other Pheasant genera (Chrysolophus and Lophura), or from one Quail genus (Coturnix). Thus the DNA of three Junglefowl species closely related to Gallus gallus lacked RAV-O sequences while the DNA of more distantly related Phasianus species showed significant homology. These results show that RAV-O-related sequences have not diverged together with the normal host genes during the evolution of the Phasianidae. Although RAV-O sequences are endogenous in all domestic chickens and Red Junglefowl studied thus far, it appears that the RAV-O genome has been introduced relatively recently into the germ line of Gallus gallus, following speciation but before domestication, and independently of the related sequences found in members of the genus Phasianus. ^^ERV missing in multiple closely related bird species Retroviral diversity and distribution in vertebrates. http://www.ncbi.nlm.nih.gov/pubmed/9621058?dopt=Abstract&holding=f1000,f1000m,isrctn We used the PCR to screen for the presence of endogenous retroviruses within the genomes of 18 vertebrate orders across eight classes, concentrating on reptilian, amphibian, and piscine hosts.... There was also some indication that viruses isolated from individual vertebrate classes tended to cluster together in phylogenetic reconstructions. This implies that the horizontal transmission of at least some retroviruses, between some vertebrate classes, occurs relatively infrequently. ^^ERV's shared among distant taxa - HGTlifepsy
March 13, 2013
March
03
Mar
13
13
2013
08:02 PM
8
08
02
PM
PDT
So Genomicus, it doesn't bother you in the least when the math, experimental, and empirical, evidence 'predicts' that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life??? And since you deny the relevance of math, experiment, and empirics any relevance to forming a basis for neo-Darwinism, please tell me exactly why you consider yourself to be 'scientific' in such rampant story telling on ERV's or anything else in the genome?bornagain77
March 13, 2013
March
03
Mar
13
13
2013
07:44 PM
7
07
44
PM
PDT
sterusjon:
I do not understand why you think the noted distribution of shared ERVs is at variance with what niwrad has proposed in LPA. I fail to see any reason that code incorporated into primates (for what reason we may not be able to discern but related to their primate-ness) would be expected or required to be included in dogs under LPA. What am I missing?
This is not the problem I'm seeing. The problem is that the pattern of ERV distribution fits with what we'd predict from common descent but does not fit with the LPA model. If common descent was true, then if an ERV sequence is shared between dogs and humans, we would predict that the vast majority of other mammals would also have this ERV sequence in the same genomic region. This is indeed what we see. On the other hand, the LPA model does not make this prediction, and can only explain this pattern with ad hoc formulations. There are other problems I am seeing with the LPA model at the molecular level (beyond the very real problem that it may not make any real predictions), which I might detail in an article on my website. Maybe.Genomicus
March 13, 2013
March
03
Mar
13
13
2013
07:29 PM
7
07
29
PM
PDT
niwrad:
LPA doesn’t exclude at all that at the corporeal run-time layer genomic material (also viruses, retroviruses, etc.) be exchanged (and eventually become ERVs or provirus and pass to offspring) between kinds (and their variants trees). It is possible that, at this layer, ERVs be shared between humans and chimps and not shared between humans and dogs (likely for complex reasons related to the proximity of humans and chimps just at the design level – after all, as body, chimps are the animals more similar to humans – nobody deny that).
I'm not quite sure I'm following you. Are you saying that the reason we don't find any instances of ERV sequences shared only between humans and dogs (but not chimps) is because of "complex reasons related to the proximity of humans and chimps just at the design level"? Yet this seems to me be ad hoc. What precisely is it in the LPA model that excludes the possibility of the designers implementing ERVs in two different organisms?
I see no principle reasons why, in LPA, prokaryotic cells cannot have, just at the design level, functional but unnecessary proteins shared with eukaryotic cells. After all, dormant software in informatics is everywhere.
Sure, but it's not predicted by the LPA model, while it is predicted from front-loading. Thus, front-loading appears to me to be a superior ID hypothesis. In other words, the LPA model - like Darwinian evolution - must explain this pattern through ad hoc adjustments.Genomicus
March 13, 2013
March
03
Mar
13
13
2013
07:21 PM
7
07
21
PM
PDT
Yes Lifepsy, and this one down a bit from that,, How Can There Be Orphan Genes? 2012 Ken Weiss – Professor of Anthropology and Genetics by the way thanks for the expansion, and links, on the ERV discussionbornagain77
March 13, 2013
March
03
Mar
13
13
2013
06:30 PM
6
06
30
PM
PDT
BA77, Hmm, we were talking about them in the thread from the other day. Is this what you meant? https://uncommondescent.com/intelligent-design/when-can-a-child-understand-an-issue-more-clearly-than-two-ph-ds-combined-when-a-shibboleth-of-nde-is-at-stake/#comment-449371lifepsy
March 13, 2013
March
03
Mar
13
13
2013
06:20 PM
6
06
20
PM
PDT
Excuse my mispell,,, lifepsybornagain77
March 13, 2013
March
03
Mar
13
13
2013
06:13 PM
6
06
13
PM
PDT
lifespy, you put up some interesting links on ORFans earlier that I was going to take a closer look at when I got the time,,, I can't seem to locate them now,, do you happen to still have them handy?bornagain77
March 13, 2013
March
03
Mar
13
13
2013
06:12 PM
6
06
12
PM
PDT
I predict more links.Mung
March 13, 2013
March
03
Mar
13
13
2013
05:15 PM
5
05
15
PM
PDT
Genomicus, You keep throwing around the word predict as if you have a scientific/mathematical basis for any of your 'predictions' for what we should find in the genome. i.e. Without any mathematical basis for any 'predictions' that you are making, you are just making up stories in my book! First, from mathematical and experimental work we can scientifically 'predict' that there has not been enough time on earth for neo-Darwinian processes to find even a single functional protein:
Evolution vs. Functional Proteins - Doug Axe - Video http://www.metacafe.com/watch/4018222 Doug Axe Knows His Work Better Than Steve Matheson Excerpt: Regardless of how the trials are performed, the answer ends up being at least half of the total number of password possibilities, which is the staggering figure of 10^77 (written out as 100, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000). Armed with this calculation, you should be very confident in your skepticism, because a 1 in 10^77 chance of success is, for all practical purposes, no chance of success. My experimentally based estimate of the rarity of functional proteins produced that same figure, making these likewise apparently beyond the reach of chance. http://www.evolutionnews.org/2010/06/doug_axe_knows_his_work_better035561.html Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact - Cornelius Hunter - July 2011 Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude. http://darwins-god.blogspot.com/2011/07/response-to-comments-proteins-did-not.html
As well this severe limit includes changing an already existent protein into a slightly different function,,
When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://www.biologicinstitute.org/post/18022460402/when-theory-and-experiment-collide
But Hey Genomicus perhaps they missed something in their math and experimental work, so let's go straight to empirical evidence and see what we find: Lenski’s Long Term Evolution Experiment - after 50,000 generations - which is equivalent to somewhere around 1,000,000 years of human evolution
Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information – September 2011 Excerpt: The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT. (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).) http://www.evolutionnews.org/2011/09/richard_lenskis_long_term_evol051051.html
How about we see what happened when the ‘top five’ mutations from Lenski’s experiment were combined??? Surely now the Darwinian magic will start flowing!!!
Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations) Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually. http://www2.cnrs.fr/en/1867.htm?theme1=7
Not even a single gene or protein, Genomicus, in 50,000 generations! Negative epistasis is extremely problematic to neo-Darwinism:
The Real Barrier to Unguided Human Evolution - Ann Gauger - April 25, 2012 Excerpt: Their results? They calculated it would take six million years for a single base change to match the target and spread throughout the population, and 216 million years to get both base changes necessary to complete the eight base binding site. Note that the entire time span for our evolution from the last common ancestor with chimps is estimated to be about six million years. Time enough for one mutation to occur and be fixed, by their account. To be sure, they did say that since there are some 20,000 genes that could be evolving simultaneously, the problem is not impossible. But they overlooked this point. Mutations occur at random and most of the time independently, but their effects are not independent. (Random) Mutations that benefit one trait (are shown to) inhibit another (Negative Epistasis). http://www.evolutionnews.org/2012/04/the_real_barrie058951.html
Tell you what, let’s just forget trying to observe evolution in the lab, let’s REALLY open the floodgates and let’s see what the almighty power of neo-Darwinian evolution can do with the ENTIRE WORLD at its disposal Genomicus.
A review of The Edge of Evolution: The Search for the Limits of Darwinism The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have “invented” little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155). http://creation.com/review-michael-behe-edge-of-evolution "The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable." - Michael Behe - The Edge of Evolution - page 146 Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution “Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell–both ones we’ve discovered so far and ones we haven’t–at best extremely limited benefit, since no such process was able to do much of anything. It’s critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing–neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered–was of much use.” http://www.evolutionnews.org/2009/05/swine_flu_viruses_and_the_edge020071.html
Now Genomicus, the experimental, empirical, and mathematical work all 'predict' that neo-Darwinian mechanisms are woefully inadequate to explain all the changes you want to attribute to it, For instance:
From Jerry Coyne, More Table-Pounding, Hand-Waving - May 2012 Excerpt: "More than 6 percent of genes found in humans simply aren't found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps." Jerry Coyne - ardent and 'angry' neo-Darwinist - professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics.
Genomicus, instead of just insisting that neo-Darwinian processes fixed all those 1400 ORFan genes (ERV's or whatever), and weaving 'just so' stories for hours on in to placate you desire for Darwinism to be true, please show me the exact math, experimental, and empirical, work that what you are insisting is true for neo-Darwinism is even possible in the real world,, so that you may be considered scientific in then first place instead of just another dogmatist! supplemental notes:
Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. Response to John Wise - October 2010 Excerpt: A technique called "saturation mutagenesis"1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans--because none of the observed developmental mutations benefit the organism.
bornagain77
March 13, 2013
March
03
Mar
13
13
2013
05:00 PM
5
05
00
PM
PDT
Genomicus, You keep throwing around the word predict as if you have a scientific/mathematical basis for any of your 'predictions' for what we should find in the genome. i.e. Without any mathematical basis for any 'predictions' that you are making, you are just making up stories in my book! First, from mathematical and experimental work we can scientifically 'predict' that there has not been enough time on earth for neo-Darwinian processes to find even a single functional protein:
Evolution vs. Functional Proteins - Doug Axe - Video http://www.metacafe.com/watch/4018222 Doug Axe Knows His Work Better Than Steve Matheson Excerpt: Regardless of how the trials are performed, the answer ends up being at least half of the total number of password possibilities, which is the staggering figure of 10^77 (written out as 100, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000). Armed with this calculation, you should be very confident in your skepticism, because a 1 in 10^77 chance of success is, for all practical purposes, no chance of success. My experimentally based estimate of the rarity of functional proteins produced that same figure, making these likewise apparently beyond the reach of chance. http://www.evolutionnews.org/2010/06/doug_axe_knows_his_work_better035561.html Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact - Cornelius Hunter - July 2011 Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude. http://darwins-god.blogspot.com/2011/07/response-to-comments-proteins-did-not.html
As well this severe limit includes changing an already existent protein into a slightly different function,,
When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://www.biologicinstitute.org/post/18022460402/when-theory-and-experiment-collide
But Hey Genomicus perhaps they missed something in their math and experimental work, so let's go straight to empirical evidence and see what we find: Lenski’s Long Term Evolution Experiment - after 50,000 generations - which is equivalent to somewhere around 1,000,000 years of human evolution
Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information – September 2011 Excerpt: The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT. (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).) http://www.evolutionnews.org/2011/09/richard_lenskis_long_term_evol051051.html
How about we see what happened when the ‘top five’ mutations from Lenski’s experiment were combined??? Surely now the Darwinian magic will start flowing!!!
Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations) Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually. http://www2.cnrs.fr/en/1867.htm?theme1=7
Not even a single gene or protein, Genomicus, in 50,000 generations! Negative epistasis is extremely problematic to neo-Darwinism:
The Real Barrier to Unguided Human Evolution - Ann Gauger - April 25, 2012 Excerpt: Their results? They calculated it would take six million years for a single base change to match the target and spread throughout the population, and 216 million years to get both base changes necessary to complete the eight base binding site. Note that the entire time span for our evolution from the last common ancestor with chimps is estimated to be about six million years. Time enough for one mutation to occur and be fixed, by their account. To be sure, they did say that since there are some 20,000 genes that could be evolving simultaneously, the problem is not impossible. But they overlooked this point. Mutations occur at random and most of the time independently, but their effects are not independent. (Random) Mutations that benefit one trait (are shown to) inhibit another (Negative Epistasis). http://www.evolutionnews.org/2012/04/the_real_barrie058951.html
Tell you what, let’s just forget trying to observe evolution in the lab, let’s REALLY open the floodgates and let’s see what the almighty power of neo-Darwinian evolution can do with the ENTIRE WORLD at its disposal Genomicus.
A review of The Edge of Evolution: The Search for the Limits of Darwinism The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have “invented” little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155). http://creation.com/review-michael-behe-edge-of-evolution "The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable." - Michael Behe - The Edge of Evolution - page 146 Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution “Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell–both ones we’ve discovered so far and ones we haven’t–at best extremely limited benefit, since no such process was able to do much of anything. It’s critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing–neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered–was of much use.” http://www.evolutionnews.org/2009/05/swine_flu_viruses_and_the_edge020071.html
Now Genomicus, the experimental, empirical, and mathematical work all 'predict' that neo-Darwinian mechanisms are woefully inadequate to explain all the changes you want to attribute to it, For instance:
From Jerry Coyne, More Table-Pounding, Hand-Waving - May 2012 Excerpt: "More than 6 percent of genes found in humans simply aren't found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps." Jerry Coyne - ardent and 'angry' neo-Darwinist - professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics.
Genomicus, instead of just insisting that neo-Darwinian processes fixed all those 1400 ORFan genes (ERV's or whatever), and weaving 'just so' stories for hours on in to placate you desire for Darwinism to be true, please show me the exact math, experimental, and empirical, work that what you are insisting is true for neo-Darwinism is even possible in the real world,, so that you may be considered scientific in then first place instead of just another dogmatist! supplemental notes:
Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. PDF - article http://eebweb.arizona.edu/nachman/Suggested%20Papers/Lab%20papers%20fall%202010/Burke_et_al_2010.pdf Response to John Wise - October 2010 Excerpt: A technique called "saturation mutagenesis"1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans--because none of the observed developmental mutations benefit the organism.
bornagain77
March 13, 2013
March
03
Mar
13
13
2013
04:59 PM
4
04
59
PM
PDT
Box, yes, I was thinking about that case :) That's why I said "as a general rule" Actually it probably depends on aspects of function. Whereas some ERV's effect embryonic development, we might never expect to find identical sequences in any creatures that have different modes of reproduction. Yet sequences associated with more specialized function (like echolocation) we might expect to find in very dissimilar species that only have that specific function in common.lifepsy
March 13, 2013
March
03
Mar
13
13
2013
04:47 PM
4
04
47
PM
PDT
Lifespy: As a general rule, I don’t think anyone predicts identical sequences found in only two morphologically or physiologically dissimilar species and none others.
Is convergence in echolocation ability in bats and whales an example? "our findings suggest that the high-frequency acoustic sensitivities and selectivities of bat and whale echolocation appear to rely on a common molecular design of prestin."Box
March 13, 2013
March
03
Mar
13
13
2013
04:34 PM
4
04
34
PM
PDT
The key phrase here is “with a subsequent loss in one species.” This is not an improbable event. Species lose genomic data relatively often.
I believe there are similar studies showing loss in multiple species, I will have to dig up. Where is the cut-off point to where the probable becomes improbable? Does such criteria exist?
The question, then, remains: why is it that we have not yet found an ERV sequence shared only between humans and dogs, or humans and cats, or cows and chimps? Etc.
Well, I was speaking more of a sequence found in humans and lower mammals, but not any other primates, or not in other mammal orders in between. Or similar examples across taxa. As a general rule, I don't think anyone predicts identical sequences found in only two morphologically or physiologically dissimilar species and none others.lifepsy
March 13, 2013
March
03
Mar
13
13
2013
04:14 PM
4
04
14
PM
PDT
Genomicus, Sorry. Sometimes it is difficult to know/remember where everyone’ sympathies lie. Witness the recent antics of Chance Ratcliff. (Chance, I got a good laugh out of all of it. You have the caricature down pat. Very creative.) Now, I am confused in another way.
The question, then, remains: why is it that we have not yet found an ERV sequence shared only between humans and dogs, or humans and cats, or cows and chimps? Etc. Think about it.
I do not understand why you think the noted distribution of shared ERVs is at variance with what niwrad has proposed in LPA. I fail to see any reason that code incorporated into primates (for what reason we may not be able to discern but related to their primate-ness) would be expected or required to be included in dogs under LPA. What am I missing? Stephensterusjon
March 13, 2013
March
03
Mar
13
13
2013
04:13 PM
4
04
13
PM
PDT
Based on this data, certain cases of widespread and similar retroviral genes are attributed to convergent evolution. Interestingly, it seems these ERVs are ordered by usefulness in placental function, and not by common descent. This is a phenomenon predicted by common design.
However, the convergence isn't at the sequence level. In other words, the ERV sequences aren't located in the same genomic loci across different taxa. This is what matters here, and I probably should have clarified that earlier. When I say "an ERV sequence shared only between humans and dogs," I mean an ERV sequence found in the same genomic location. Again, why don't we see that?Genomicus
March 13, 2013
March
03
Mar
13
13
2013
03:27 PM
3
03
27
PM
PDT
Genomicus,
To put this differently: if we find the same ERV in a dog and human, we can predict, based on common descent, that chimps will also have this ERV. But if we find an ERV shared between chimps and humans, we cannot predict we will find this ERV in dogs.
From ancestral infectious retroviruses to bona fide cellular genes: role of the captured syncytins in placentation. http://www.ncbi.nlm.nih.gov/pubmed/22695103 We focus on the recent discovery of genes derived from the envelope glycoprotein-encoding (env) genes of endogenous retroviruses that have been domesticated by mammals to carry out an essential function in placental development... Remarkably, the capture of syncytin or syncytin-like genes, sometimes as pairs, was found to have occurred independently from different endogenous retroviruses in diverse mammalian lineages such as primates--including humans--, muroids, leporids, carnivores, caviids, and ovis, between around 10 and 85 million years ago. Retroviruses push the envelope for mammalian placentation http://www.pnas.org/content/109/7/2184.short Domestication of the syncytin genes represents a dramatic example of convergent evolution via the cooption of a retroviral gene for a key biological function in reproductive biology. In fact, syncytin domestication from a retroviral envelope gene has been previously shown to have independently occurred at least seven times during mammalian evolution... Based on this data, certain cases of widespread and similar retroviral genes are attributed to convergent evolution. Interestingly, it seems these ERVs are ordered by usefulness in placental function, and not by common descent. This is a phenomenon predicted by common design.lifepsy
March 13, 2013
March
03
Mar
13
13
2013
03:15 PM
3
03
15
PM
PDT
Eric has previously noted the evolutionist propensity for failure to note that the paradigm shift requires a shift in the thought process.
Since I'm an ID proponent, I'm quite adept at shifting into the ID perspective. Actually, I'm in the ID perspective virtually all of the time.
In that vein, are you so fixated on the evolutionary explanations and how good you think they are that you are incapable of shifting your perspective and meeting the LPA proposal on its own terms?
What exactly do you mean by "meeting the LPA proposal on its own terms"? The LPA view of life has been proposed; I'm bringing up biological data that seem to conflict with the LPA view. It is, of course, good to see that you all are actually beginning to think about and propose ID hypotheses (no disrespect intended, but I am slightly frustrated by the obsession with critiquing Darwinian evolution instead of proposing a testable ID hypothesis). However, in my humble opinion, this particular view (the LPA model) looks awfully ad hoc. Put differently, I am having difficulty thinking of any actual, hard predictions it might make (contrast this with, e.g., the front-loading hypothesis).Genomicus
March 13, 2013
March
03
Mar
13
13
2013
03:06 PM
3
03
06
PM
PDT
To clarify, I’m referring to an ERV fixed at the root of a primate tree, but missing in only certain descendents. Conservation and loss of the ERV3 open reading frame in primates. http://www.ncbi.nlm.nih.gov/pubmed/15081124 ERV3 sequences were amplified by PCR from genomic DNA of great ape and Old World primates but not from New World primates or gorilla, suggesting an integration event more than 30 million years ago with a subsequent loss in one species. Now to what extent is this incongruence permitted? If you can excuse it in primate lineages, what difference does it make to extend further down the tree? Where is the cut-off point for falsifiability, and what empirical criteria determines this?
The key phrase here is "with a subsequent loss in one species." This is not an improbable event. Species lose genomic data relatively often. Now then, suppose we found a particular ERV sequence only in dogs and humans. This would be quite a significant find, because it would mean that those ERV sequences of all other mammalian species were independently lost. Unless the ERV sequence is deleterious in nature, this is a staggeringly improbable occurrence. The question, then, remains: why is it that we have not yet found an ERV sequence shared only between humans and dogs, or humans and cats, or cows and chimps? Etc. Think about it.Genomicus
March 13, 2013
March
03
Mar
13
13
2013
03:00 PM
3
03
00
PM
PDT
1 2 3

Leave a Reply